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目的 通过腺苷 (ADO)受体拮抗剂 茶碱 (TH) ,探讨ADO、双哌达莫 (DPM)对小鼠肺间质纤维化过程的干预作用。方法 1 0 0只小鼠经气道注入博莱霉素 (BLM ,8.5mg/kg)制备肺纤维化动物模型 ,随机分成BLM、DPM、ADO和TH 4组 ,分别给予生理盐水 (1 0 0 μl/d)、DPM (50mg·kg- 1 ·d- 1 )、ADO(50mg·kg- 1 ·d- 1 )、DPM和TH (50mg·kg- 1 ·d- 1 ) ,共 7天 ,第 4～ 30天内处死动物 ,观察肺超微结构与病理变化。结果 BLM组肺泡上皮细胞坏死多 ,内皮伸出许多长棘突呈现肺组织缺氧 ,1 0天后间质出现大量成纤维细胞 ,因胶原增加伴炎症细胞浸润导致肺泡隔增宽 ;第 2 0天后DPM和ADO两组与BLM组比较 ,坏死肺泡上皮细胞少 ,第 4～ 30天活跃的肺泡巨噬细胞 (AM)数量增多 ,胞质内含大量溶酶体与吞饮小泡 ,第 30天塌陷肺泡与成纤维细胞均减少 ;TH组坏死肺泡上皮细胞很多 ,毛细血管闭锁、因肺组织缺血 ,间质内浸润的单核细胞发育成巨噬细胞延迟 ,成纤维细胞很少。结论 BLM能损伤肺泡上皮细胞致缺氧是成纤维细胞大量增生的重要因素之一 ,DPM与ADO通过改善微循环 ,促进AM发育和肺泡腔重建 ,以抑制成纤维细胞的增生
Objective To investigate the intervention of ADO and dipyridamole (DPM) on pulmonary interstitial fibrosis in mice by theophylline (AD) receptor antagonist TH. METHODS: Pulmonary fibrosis model was established by injecting bleomycin (BLM, 8.5mg / kg) into the lung of rabbits. The rats were randomly divided into three groups: BLM, DPM, ADO and TH 4 groups. DPM (50 mg · kg -1 · d -1), ADO (50 mg · kg -1 · d -1), DPM and TH (50 mg · kg -1 · d -1) for 7 days, Animals were sacrificed on days 4 to 30 to observe lung ultrastructure and pathological changes. Results The alveolar epithelial cells were more necrotic in BLM group than in control group. Many long spinous processes in the endothelium showed hypoxia in the lung tissue. After 10 days, a large number of fibroblasts appeared in the stroma, and the alveolar septa broadened due to increased collagen and infiltration of inflammatory cells. After 20 days Compared with the BLM group, the number of necrotic alveolar epithelial cells in DPM and ADO groups was less than that in BLM group. The number of active alveolar macrophages (AM) in the 4th to 30th days increased, the cytoplasm contained a large amount of lysosomes and swallowing vesicles, and on the 30th day Collapsed alveoli and fibroblasts were reduced; TH group necrosis alveolar epithelial cells, capillaries atresia, due to lung ischemia, interstitial infiltration of mononuclear cells into macrophages, fibroblasts rarely. Conclusion BLM can damage the alveolar epithelial cells induced hypoxia is one of the important factors of fibroblast proliferation, DPM and ADO by improving microcirculation, promote AM development and alveolar remodeling, in order to inhibit fibroblast proliferation